The effects of centrally injected arachidonic acid on respiratory system: Involvement of cyclooxygenase to thromboxane signaling pathway

Erkan L. G., Guvenc G., Altinbas B., Niaz N., YALÇIN M.

RESPIRATORY PHYSIOLOGY & NEUROBIOLOGY, vol.225, pp.1-7, 2016 (SCI-Expanded) identifier identifier identifier

  • Publication Type: Article / Article
  • Volume: 225
  • Publication Date: 2016
  • Doi Number: 10.1016/j.resp.2015.12.010
  • Journal Indexes: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Page Numbers: pp.1-7
  • Keywords: Arachidonic acid, Cyclooxygenase, Thromboxane A2, Tidal volume, Respiratory rate, Respiratory Minute Ventilation, Partial oxygen pressure, Partial carbon dioxide pressure, Intracerebroventricular, HEMORRHAGED HYPOTENSIVE RATS, PHOSPHOLIPASE A(2) ACTIVATOR, CENTRAL HISTAMINERGIC SYSTEM, PERIPHERAL MECHANISMS, BREATHING MOVEMENTS, FETAL LAMBS, MELITTIN, CASCADE, PRESSOR
  • Bursa Uludag University Affiliated: Yes


Arachidonic acid (AA) is a polyunsaturated fatty acid that is present in the phospholipids of the cell membranes of the body and is abundant in the brain. Exogenously administered AA has been shown to affect brain metabolism and to exhibit cardiovascular and neuroendocrine actions. However, little is known regarding its respiratory actions and/or central mechanism of its respiratory effects. Therefore, the present study was designed to investigate the possible effects of centrally injected AA on respiratory system and the mediation of the central cyclooxygenase (COX) to thromboxane A2 (TXA2) signaling pathway on AA-induced respiratory effects in anaesthetized rats. Intracerebroventricular (i.c.v.) administration of AA induced dose- and time-dependent increase in tidal volume, respiratory rates and respiratory minute ventilation and also caused an increase in partial oxygen pressure (pO2) and decrease in partial carbon dioxide pressure (pCO2) in male anaesthetized Sprague Dawley rats. I.c.v. pretreatment with ibuprofen, a non-selective COX inhibitor, completely blocked the hyperventilation and blood gases changes induced by AA. In addition, central pretreatment with different doses of furegrelate, a TXA2 synthesis inhibitor, also partially prevented AA-evoked hyperventilation and blood gases effects. These data explicitly show that centrally administered AA induces hyperventilation with increasing pO2 and decreasing pCO2 levels which are mediated by the activation of central COX to TXA(2) signaling pathway. (C) 2016 Elsevier B.V. All rights reserved.